During the coming year we would like to elucidate the mechanism by which calcium movement from the mitochondria to the cytosol of liver cells increases gluconeogenesis. Now that a highly active and homogeneous preparation of PEPCK is available, we will again investigate the interaction between the ferroactivator and the pure enzyme. Finally, we will undertake an investigation of the mechanisms by which Fe2 ion is provided to liver cytosolic ferroactivator so that PEPCK can be "turned on". We will try to determine the cell locus that supplies the iron, the mechanisms by which it is released to ferroactivator, and the possible role of redox systems in determining whether the Fe is in the 2 plus or 3 plus state.